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MBBS VI Medicine > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What are the layers of epithelium (from surface to basal)

A
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2
Q

What are the 3 layers in skin?

A

Epidermis: basement membrane/dermoepidermal junction
Dermis
Subcutaneous tissue/subcutis

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3
Q

What is the function of the epidermis?

A
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4
Q

What is common disease of epidermis?

A
  • SJS
  • Toxic epidermoid necrolysis
  • Eyrthroderma
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5
Q

What are the layers of basement membrane/dermoepidermal junction?
What is function of DEJ?

A

-Basal cell membrane-Lamina lucida (20-40nm)-Lamina densa (30-60nm)-Sub-lamina densa + Anchoring fibrils

Function of DEJ
-Mechanical support
-Adhesion
-Growth of basal layers

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6
Q

What are common diseases of DEJ?

A

Hereditary: junctional and dystrophic epidermolysis bullosa (complex inherited idseases p/w friable skin, bullous lesion, often w/scaring)
Acquired: bullous pemphigoid: antihemidesmosomal ab produced and appear to induce inflammation and subseqent damage of hemidesmosomes, causing blsiter to develop between cells and BM. Blistering occurs secondary to disruption of structures of BM and dermis

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7
Q

What are the layers of the dermis? (from surface to basal)
Functions of dermis?

A

Layers
Papillary dermis: finger like projection in contact with Rete ridges
Reticular dermis: dermal plexus (dermis is rich in blood supply), dense connective tissue)

  1. Thermoregulation -Through control of cutaneous blood flow and sweating, achieved by dermal vessels and eccrine sweat glands 2.Mechanical protection
    -Primarily by Collagen and Hyaluronic acid
  2. Innervation of the skin
  3. -Responsible for cutaneous sensation
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8
Q

What is the pilosebacous unit composed of, what common diseases affecting pilosebaceous unit?

A

Consists of hair follicle, sebaceous gland, hair

Common disease affecting pilosebaceous unit: acnes

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9
Q

What is eccrine glands
What disease affects eccrine glands?

A

Eccrine glands -Watery sweat glands-Millions of eccrine glands in human body-Widely distributed all over body esp. Palms, Soles

Secretory activities-Ultra-filtrate of plasma-like fluid-Hypotonic sweat

Common diseases affecting Eccrine glands-Cystic Fibrosis: Defective ductal Na reabsorption

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10
Q

What are the structural components of nail?

A
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11
Q

What are barrier defects in skin?
What complications?

A
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12
Q

What is the pathogenesis of defective stratum corneum?

A
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13
Q

What is the disease of allergen barrier in skin?
What pathophysiology and gene involved?

A

-Aetiology: Filaggrin gene mutation; House dust mites, feathers-

Pathophysiology: *Lack of Ceramides (Sphingolipids) (common lipid in cells)

*Trans-epidermal water loss increase → Skin cracks → Allergen enter → Epi-cutaneous sensitisation by allergies

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14
Q

What is the classical and alternative pathway?

A

C3a,4a,5a are anaphylatoxin (vasodilation and vascular permeability)
C3b: opsoniziation of bacteria (marking) + induce phagocytosis
C5a: anaphylatoxin (mast cell release histamine); neutrophil chemotaxis

C5b + C6-9: MAC –> makes pores in cell membrane –> osmotic lysis

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15
Q

What is the lectin pathway>

A

(Microbial carbohydrates) *Lectin-Mannose:-C2 → C2a + C2b-C4 → C4a + C4b

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16
Q

What is antimicrobial peptides on skin
What disease associated with increased expression?

A

-Secreted from epidermis-e.g. Human beta-defensins (HBD-1 to HBD-4), Dermocidine-Anti-bacterial/ viral/ mycotic properties

-Psoriasis * Increased expression of HBD-2 *Less bacterial infection observed in Psoriasis patients

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17
Q

What is cells involved with adaptive immunity?

A
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18
Q

What is erythematous?
What are common erythematous lesions?

A

-Blanchable skin redness due to vasodilatation (+/- inflammation) Common Erythematous lesions
-Atopic Dermatitis
-Psoriasis
-Skin infections

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19
Q

What is violaceous
What are common violaceous lesions

A

-Purplish-Lichenoid eruption *Lichen planus, Rheumatological, Lichenoid drug eruption *Graft-versus-host disease of skin Common Violaceous lesions
-Petechiae
-Purpura

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20
Q

What are hyperpigmented lesions and common examples?

A
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21
Q

What are hypopigmented lesions and common examples?

A
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22
Q

What are skin diseases with well defined borders?

Ill defined borders

A

Well defined borders
Psoriasis
Tinea corporis
Vitiligo

Ill defined borders
* Atopic dermatitis
* Viral exanthema
* Drug eruption/exanthema

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23
Q

What are common causes for flat lesions: macule and patch?

A
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24
Q

What are common causes for raised lesions?
Papule
Plaques
Common hweals
Common nodules
Common skin tumors

A
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25
Q

How to describe a raised, palpable fluid filled skin lesion?

A

*Vesicle/ Bleb: Clear content, <0.5cm
*Blister/ Bulla: Clear content, ≥0.5cm
*Cyst: Clear content, Deep involvement
*Pustule: Purulent content; <0.5cm
*Abscess: Purulent content; >0.5cm

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26
Q

What are causes of common vesicles?

A

-Herpes Simplex
*Eczema Herpeticum (Skin HSV infection due to contaminated contact with Herpes; Eroded vesicles)
-Chickenpox/ Varicella
-Herpes Zoster/ Shingles (usu. dermatomal)

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27
Q

What are common causes of blisters?

A

-Pemphigus
-Bullous Pemphigoid
-Steven Johnson Syndrome

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28
Q

What are common causes of pustules?

A

-Skin infection e.g. Impetigo -Pustular Psoriasis-Acute generalised exanthematous pustulosis (AGEP)-Sub-corneal pustulosis-IgA pemphigus

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29
Q

How to describe bleeding into skin?

A
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30
Q

How to describe the different disruptions of skin surface?

A
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31
Q

What are the common causes of crust?

A

Crust: a collection of cellular debris, dried serum, blood
-A scab antecedent primary lesion is usu. vesicle or pustule Common causes of Crust
-Herpes Simplex
-Impetigo

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32
Q

What is scaling of skin?
Common causes?

A
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33
Q

What is the histological classification of skin scaling?

A
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34
Q

Define lichenificiation
Common causes?

A
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35
Q

Define scar clinical characteristics
What is atrophy

A
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36
Q

What is an annular lesion
What are common annular lesions?

A
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37
Q

How to describe targetoid lesions?
What is it hinting to?

A

Inner erythematous ring + outer pale ring
Hinting erythema multiforme

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38
Q

What is maculopapular exantham
ddx?

A

-Widespread rash all over skin (Exanthem) with mixed erythematous flat (Macules) and raised (Papules) lesions-Spared mucosa (c.f. Enanthem) -“Maculopapular” is only used in this particular presentation
-Ddx
*Measles
*Rubella *
Erythema infectiosum
*Roseola infantum
*Drug eruption

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39
Q

What are the cause of punched out, monomorphic erosiosn?

A

Raised erythematous lesions (vesicles) but punctuated = appearance of punched out
Hint = eczema herpeticum: fulminant HSV infection on re-existing atopic dermatitis
p/w ever and widespread punctate vesicles
Can be complicated by impetigo –> pustules, golden yellow crests

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40
Q

What is cause of monomorphic papules and pustules

A

Hint Pityrosporum folliculitis

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41
Q

What is cause of polymorphic Papules, Nodules, Scars, Comedones

A

Acne vulgaris

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42
Q

What is etiology of psoriasis
What is environmnetal precipitation
What are the clinical associations?

A

Genetic predisposition: PSROS1 in MHC1 gene on chromosome 6

Environmental precipitation
* Alcohol intake
* Drugs e.g. hydroxychloroquine, terbinafine, lithium
* Stress
* Streptococcal infection –> acute guttate psoriasis or pustular psoriasis
* HIV infection

Clinical associations
* 15% patients with cutaneous psoriasis has psoriatic arthropathy
* Obesity
* Smoking
* DM
* HT
* HF
* MI
* CVD e.g. CAD, stroke, PE

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43
Q

What is the pathogenesis of psoriasis
What is the histopathology?

A

Pathogenesis
* Genetic predisposition + precipitated by infective/environmental triggers
* Stimulus –> activation of dendritic cells and T cells –> formation of an immunological synapse that enhances their interactions –> vicious cycle
* Results in release of cytokines, chemokines and growth factors that trigger keratinocyte proliferation, altered differentiation, and angiogenesis. Within the chronic psoriatic plaque, a vicious cycle of continuous T cell and dendritic cell activation is envisioned

Histopathology
* Acanthosis
* Hyperkeratosis (parakeratosis)
* Superficial perivascular dermatitis
* Munros microabscess = neutrophil remnant accumulating in subcutaneous tissue
* Spongiform pustule of Kogoj = spone like intraepidermal neutrophil filled abscess

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44
Q

What is the classification of psoriasis?

A
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45
Q

What is the appearance of psoriasis vulgaris?
What is the distribution of lesions?

A
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46
Q

What is the appearance of pustular psoriasis?
What is the distribution of lesions?
Management?

A
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47
Q

What is the appearance of psoriatic erythroderma/erythrodermic psorasisi?
What is the distribution of lesions?

A
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48
Q

What are the nail manifestations of psoriasis

A
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49
Q

What is 1st line, 2nd line management of psoriasis?

A
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50
Q

What are the indications for 3rd line systemic treatment for psoriasis?
What are the options?

A
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51
Q

What is etiology of atopic dermatitis?
What are the environmental precipitations?

A

Genetic predisposition
Filaggrin gene mutation: missense mutation –> lack of ceramides (lipid in cells)
presence of other atopic disease: cutaneous sensitization causes sensation in other epithelial barriers e.g. airway, nasal cavity. May explain phenemenon in eczema –> asthma –> rhinoconjunctivitis
Wiskott Aldrich syndrome

Environmental precipitation
* Allergen: house dust mite, pets, drugs, alcohol
* Irritiants: soap, detergent, washing powder, spicy food, fabrics, solvents
* Stress
* Climate (humidity, warmth) and sweating
* Infection

52
Q

Pathogenesis of atopic dermatitis
Histology

A

Pathogenesis
* Lack of cermadies –> increased transepidermal water loss –> skin cracks –> allergen exposure
* IgE mediated immune response (increased serum total and Ag specific IgE)
* Polarization of naive T cells. acute contact: Th2 response. Chronic contact: Th1 response (cell mediated) + skin remodelling –> increased IgE bearing Langerhans cells and inflammatory dendritic cells

Eczema flares: biphasic reaction upon antigen exposure in senzitized patients
early phase (within 15 min): mast cell degranulation –> histamine release –> pruritis/itch
Late phase: eosinophil, basophil, monocyte, lymphocyte –> skin macules

Histology
* Orthrokeratosis
* Hypergranulosis
* Intra-epidermal edema (spongiosis/intercellular edema)
* Superficial perivascular dermatitis
* Lymphocyte and eosinophil infiltration

53
Q

What is the triphasic progression of atopic dermatitis?

A

-Acute phase: Erythematous, Vesicular, Exudative, Crusting
-Subacute phase: Disc-shaped lesions
-Chronic phase: Dry and Scaly, Lichenification, Hyper-pigmented

54
Q

What is the distribution of atopic dermatitis in infants, childhood and adolescent/adults?

A
55
Q

What are the associated coinfections with eczema?

A
56
Q

How to make dx of atopic dermatitis?

A
57
Q

What are the different steps in management of atopic dermatitis?

A

-Treat underlying/ secondary infection
-1st line: Avoidance of irritants/ allergens, Emollient , Antiseptic bath (with diluted bleach for S. aureus colonisation), Probiotics, Topical steroids, Antihistamine, Potassium permanganate
-2nd line: Topical Calcineurin inhibitor (Tacrolimus, Pimecrolimus), Wet wrap
-3rd line: Phototherapy, MMF, Cyclosporine, Azathioprine, Systemic Steroid
-Novel treatment: IL4 & IL13 inhibitor (Dupilumab)

58
Q

What are the different topicals steroids that are used for atopic dermatitis?
What are hte associated ADR?

A
59
Q

What is the pathogenesis of contact dermatitis?
What is clinical presentation?

A

Pathogenesis
Sensitization phase: T cells develop specific memory CD4 T cells upon presentation of Hapten with Langerhans cells which engulfed allergens from skin
Eliciting phase: cytokines released by CD4 –> vessel extravasation

Clinical presentation
* Skin itchiness
* Skin erythematous patch: usu well defined, scaly surface
* Acute: slow discharge, vesicles

60
Q

What tests do make dx of contact dermatitis
What are the indications to do ix?

A
61
Q

What is the clinical feature of seborrheic dermatitis?
How to differentiate from atopic dermatitis?
Management?

A
62
Q

What is etiology of urticaria?
Clinical presentation?

A
63
Q

What is acute urticaria
Chornic urticaria

A
64
Q

How to make dx of urticaria?
What is management of urticaria?

A
65
Q

What is etiology of erythroderma?
What is the clinical criteria?

A
66
Q

How to make dx of erythroderma?
What is the management of erythroderma?

A
67
Q

What are the common and uncommon causes of erythema nodosum?
What is clinical presentation of EN?

A
68
Q

What is histology of erythema nodosum?

A

A type of panniculitis, septal w/o vasculitis

  • Septal panniculitis
  • Subcutaneous septal edema
  • Fibroplasia (chronic)
  • Neutrophil +/-eosinophil infiltration
69
Q

What are the common and uncommon caues of erythema induratum?
What is the clinical presentation?

A

Panniculitis, lobular w/ vasculitis (differs from erythroderma nodosum which has no associated vasculitis)

70
Q

What is the clinical presentation of lipodermatatosclerosis?

A

Severe venous insufficiency –> venous hypertension

71
Q

What is the distribution of pancreatic panniculitis?

A
72
Q

What are the types of cutaneous lymphoma?

A
73
Q

What is the etiology of erythema multiforme?

A
74
Q

What is the classification of erythema multiforme?

A
75
Q

What is the clinical presentation of erythema multiforme?
What are complications?
What are ocular manifestatins?

A
76
Q

What is the management of erythema multiforme?

A
77
Q

What is the classification of cutaneous lupus erythematosus

A
78
Q

What is the histology of CLE (cutaneous lupus erythematosus)?

A
79
Q

What is management of cutaneous lupus erythematosus?

A

Topical treatment
Steroids: useful in all forms of CZLE
Calcineurin inhibitors (tacrolimus) may be used in DLE, SCLE, ALE: steroid sparing effect
Intralesional steroid: may be used in localized lesions of DLE, tumid LE, lupus panniculitis

Systemic treatments: antimalarials (Drug of choice for all types of CLE)
AE: GI upse,t skin dyspigmentation, ocular changes: bulls eye maculopathy (with chloroquine; now rare). reversible corneal deposits, irreversible retinopathy

80
Q

What is the etiology of subacute CLE (SCLE = subacute cutaneous lupus erythematosus)?
What is the clinical presentation?
What serology should be done to assist in dx?

A

50% have 4+ features that classify them for a dx of SLE

81
Q

What is the etiology of discoid lupus erythematosus (DLE)?
What are the types?
How to make dx of DLE?

A

Types
* Disseminated DLE: lesions above and below neck
* Localized DLE: lesions limited to H&N region (most commonly face. Other areas: scalp, ext ear canal, conchal bowl, V neck, extensors of arms. Spares nasolabial folds)
* Mucosal DLE (can be oral mucosal)

Dx
* ANA +ve (25%)
* Direct IF +ve (60%)
* +ve lupus band test in non lesions skin may be predictive of possible conversion to systemic disease
* In scarring alopecia caused by DLE, deposits are around the hair follicles

82
Q

What is clinical presentation of Chilblain lupus erythematosus
What is associated condition?
How to make dx?

A
83
Q

What is clinical presentation of Tumid LE (lupus erythematosus)?
How to make dx?

A
84
Q

What is clinical presentation of Tumid LE (lupus profundus/lupus panniculitis)?
How to make dx?

A
85
Q

What is lichen planus?
What histology?

A
86
Q

What is the etiology of rosacea?
What is the classification of rosacea?
What is the clinical presentation?

A
87
Q

What is the clinical presentation of pityriasis rubra pilaris?

A

-Reddish orange scaly plaques
-Palmoplantar keratoderma
-Keratotic follicular papules

88
Q

What is the classification of pemphigus?

A
89
Q

What is the clinical presentation of pemphigus?
What is the dx?

A
90
Q

What is the management of pemphigus?

A

-Systemic Steroid, Mycophenolate mofetil, Azathioprine, Cyclophosphamide, Cyclosporine
-Plasmapheresis, IVIG

91
Q

Compare pemphigus vs bullous pemphigoid in pathogenesis, distribution, histology and serum Ab.
Associated conditions
Management
Prognosis

A

Lesions: bullous pemphigoid are subepidermal and hence unlikely to erode in comparison to pemphigus vulgaris: intraepidermal so weak and rupture easily resulting in painful erosions

Nikolsky sign: typically negative in bullous pemphigoid and often positive in pemphigus vulgaris

92
Q

What is the clinical presentation of bullous pemphigoid?
What is the histology?
What is the management?

A
93
Q

What is the pathogens causing impetigo?
What is complication?
Management?

A
94
Q

What is the pathogens causing erysipelas?
What is the clinical presentation?

A
95
Q

What layer does cellulitis affect?
What is the pathogens causing cellulitis?
What is the clinical presentation?

A
96
Q

What is the spectrum of progression of pyoderma
What are the main pathogens affecting this condition
What is the management?

A
97
Q

What is the pathogen causing erythrasma?
What is the clinical presentation?
What is the Ix done?
Management?

A
98
Q

What is the classification of necrotizing fasciitis?
What are the RF?

A
99
Q

What is the pathogenesis of necrotizing fasciitis?
Clinical presentation?

A
100
Q

Compare clinical presentation of necrotizing fasciitis vs cellulitis

A
101
Q

What is the management of necrotizing fasciitis?

A

-Fluid resuscitation/ Blood transfusion
-Surgical exploration
-Surgical debridement of all avascular skin and fascia
-IV Abx e.g. Gentamicin, Fortum (Poor response to oral Abx)

102
Q

What is cause of clostridial myositis (gas ganrene)
What is clinical presentation
What is management?

A

Pathogen: clostridium peprfringens, other clostridium spp. Facultative anaerobes e.g. enterobacteriaceae
Pathogenesis: muscle injury with soil/foreign material contamination –> colonization by clostridial spores –> coagulative necrosis of muscle (thus myonecrosis)

Clinical presentation
* Rapidly progressive severe pain
* Wound purulent discharge: sero-sanguineous (pus + blood)
* Crepitus felt beneath skin
* Septic shock
* Compartment syndrome

Management
* Urgent surgery
* IV Abx
* Hyperbaric oxygen chamber

103
Q

What is cause of SSSS?
What is clinical presentation?
Ix to make Dx?
What is management?

A
104
Q

What are the types of cutaneous TB?

A
105
Q

What is pathogenesis of acne vulgaris?

A
106
Q

What is clinical presentation of acnes?

A
107
Q

Etiology of herpes simplex
Clinical presentation

A
108
Q

What are skin warts?
Management?

A
109
Q

What is virology of molluscum contagiosum
Clinical presentation
Management

A
110
Q

What is virolgy of VZV?
Pathogenesis

A
111
Q

Clinical presentation of VZV
Complications of varicella

A
112
Q

Ix for varicella

A
113
Q

What is the clinical presentation of shingles?
What specific herpes zoster syndromes?
What complications?

A

Neuropathic pain due to neuritis
Classically maculopapular rash that evovles into vesicles or pustules
Erythematous macules –> papules –> vesicles –> pustules –> ulceration and crusting
In distribution of unilateral dermatome. Mostly affect T3-L3 dermatomes

Ramsay hunt syndrome/herpes zoster oticus
* CN7: rash in external auditory canal, facial nerve palsy
* CN8: burning otalgia, allodynia
Herpes zoster opthalmicus
* Latent VZV infection trigeminal ganglion –> reactivation in CNV1
* Hutchingson sign in prodromal period (vesicles in the nose area due to activation of nasociliary branch of CNV1)
* Periorbital rash: keratitis, uveitis, conjunctivitis, debilitating pain, visual loss (MUST ASK ABOUT EYE PAIN –> refer to ophtalmology)

Complications
* Post herpetic neuralgia
* CNS complications: meningitis. encephalitis, granulomatous angiitis (VZV vasculopathyu or stroke)

114
Q

What is the use of antiviral in shingles?
What is the timing for use of antivirals?
How does complicated VZV infections guide management?

A

Effect: accelerate healing of lesions (reduce scarring), decrease duration and severity of pain

Timing: recommnede <72h of clinical symptoms for max benefit: still reommended >72h if new lesions are appearing at the time of presentation (indicate ongoing viral replication); unknown utility of antiviral >72h after onset, likely minimal benefit

115
Q

What are the common species causing dermatophysis/tinea?

A

-Epidermophyton - affect nails and skin
-Microsporum - affect hair and skin
-Trichophyton - affect hair, nails and skin

116
Q

What is the classification of dermatophytosis?

A

-Tinea capitis = Scalp
-Tinea faciei = Face
-Tinea corporis = Trunk & Limbs
-Tinea manuum = Hands
-Onychomycosis/ Tinea unguium = Fingernail, Toenail
-Tinea cruris = Groin
-Tinea pedis = Foot (香港腳)
-Tinea barbae = Beard

117
Q

What are the 4 main patterns of tinea pedis?

A

-Interdigital: *Erythema, Scaling, Maceration with fissures * In web spaces esp. between 4th & 5th *usu. a/w T. rubrum or T. mentagrophytes
-Moccasin *Diffuse scaling on soles extending to sides of feet *usu. a/w T. rubrum *Genetic predisposition is proposed to explain strong FHx and treatment refractoriness
-Ulcerative *usu. a/w T. interdigitale *Typically begins in the 2 lateral interdigital spaces and extends to lateral dorsum and plantar surface of arch *Lesions of toe webs are usu. macerated and have scaling borders *Sometimes complicated by secondary bacterial infection
-Vesiculobullous *usu. a/w T. interdigitale *Vesicular eruptions on arch or side of the feet *May give rise to Dermatophytid reaction (i.e. inflammatory reaction at sites distant from site of infection) e.g. Pompholyx-like hands

118
Q

What is the management of dermatophytosis?

A
119
Q

What is the cause of scabies?
What is the clinical presentation?

A

Sarcoptes scabiei

120
Q

How to make clinical dx of scabies?
What Ix may be done?

A
121
Q

Management of scabies?

A
122
Q

Diseases causing Malar Rash

What Ix done?

A

-Mucocutaneous Lupus (ACLE)
-Tumid Lupus Erythematosus
-Irritant contact dermatitis (use of new facial products, hair dye)
-Carcinoid syndrome
-Dermatomyositis
-Atopic Dermatitis

ix
-Skin biopsy for direct immunofluorescence
-Blood for ANA, Anti-dsDNA

123
Q

What are common and uncommon diseases causing panniculitis?

A
124
Q

What is the diagostic algorithm for mostly septal panniculitis in skin biopsy?

A

Primarily septal panniculitis without vasculitis: erythema nodosum is most common clinical form of panniculiaits

125
Q

What is the diagostic algorithm for mostly lobular panniculitis in skin biopsy?

A

MBBS VI Medicine (92 decks)

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